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The rheumatoid arthritis shared epitope increases cellular susceptibility to oxidative stress by antagonizing an adenosine-mediated anti-oxidative pathway
We have recently demonstrated that the rheumatoid arthritis (RA) shared epitope (SE) acts as a ligand that triggers nitric oxide (NO) signaling in opposite cells. Given the known pro-oxidative effect of NO and the proposed role of oxidative stress in the pathogenesis of RA, this study explores wheth...
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| Główni autorzy: | , , , , , |
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| Format: | Artigo |
| Język: | Inglês |
| Wydane: |
BioMed Central
2007
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| Hasła przedmiotowe: | |
| Dostęp online: | https://ncbi.nlm.nih.gov/pmc/articles/PMC1865041/ https://ncbi.nlm.nih.gov/pubmed/17254342 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1186/ar2111 |
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